Hyperlipemia is a symptom in which the lipoprotein in blood becomes abnormally excessive, and which is also strongly associated with diseases, such as arteriosclerosis and myocardial infarction, so its treatment is considered important.
Various medicines are used for the treatment of hyperlipemia, and HMG-CoA reductase inhibitors such as pravastatin, simvastatin, fluvastatin and atorvastatin are mainly used as therapeutic agents therefor. It is known that pitavastatins have a strong HMG-CoA reductase inhibiting action and are useful as a blood cholesterol-reducing agent (Japanese Patent No. 2569746, U.S. Pat. No. 5,856,336 and European Patent No. 304063).
The main components of blood lipoprotein are cholesterol and triglyceride, and the blood cholesterol level of hyperlipemic patients not only increases, but is also accompanied with an increase in triglyceride in many cases. When an HMG-CoA reductase inhibitor is administered to hyperlipemic patients, blood cholesterol is sufficiently lowered, but triglyceride is not sufficiently lowered. Besides, there is a method by which hyperlipemic patients suffering from a high level of the cholesterol and triglyceride in blood are treated by increasing an administering dose of the HMG-CoA reductase inhibitor for the purpose of lowering both of cholesterol and triglyceride. However, this method is problematic over the safety issues and therefore is not recommended.
On the other hand, eicosapentaenoic acid (EPA) is a long-chain essential fatty acid contained primarily in fish oil, and this acid is reported to serve as an inhibition in absorption of triglyceride from an intestinal tract, an inhibition in biosynthesis in a liver, a reduction in blood triglyceride by enhancing a plasma lipoprotein lipase activity (Mizuguchi, K. et al.: Eur. J. Pharmacol. 235, 221 to 227, 1993, Mizuguchi, K. et al.: J. Jpn. Atheroscler. Soc. 18 (5), 536, 1990), an inhibition in synthesis of liver cholesterol and a reduction in blood total cholesterol by an acceleration in excretion of cholesterol into bile (Mizuguchi, K. et al.: Eur. J. Pharmacol. 231, 121 to 127, 1993).